Staining Tissue From Space Mice

Our Synaptic Marker is Used to Compare Earth vs Space Samples
Exposure to the microgravity conditions of spaceflight alleviates the load normally imposed by the Earth’s gravitational field upon the inner ear utricular epithelia. Previous ultrastructural investigations showed that spaceflight induced an increase in synapse density within hair cells of the rat utricle. However, the utricle exhibits broad physiologic heterogeneity across different epithelial regions, and it is unknown whether capabilities for synaptic plasticity generalize to hair cells across its topography. To achieve systematic and broader sampling of the epithelium than previously conducted we used immunohistochemistry and volumetric image analyses to quantify synapse distributions across representative utricular regions in specimens from mice exposed to spaceflight (a 15-day mission of the space shuttle Discovery). These measures were compared to similarly-sampled Earth-bound controls. Following paraformaldehyde fixation and microdissection, immunohistochemistry was performed on intact specimens to label presynaptic ribbons (anti-CtBP2) and postsynaptic receptor complexes (anti-Shank1A) DOI: 10.1152/jn.00240.2016.

Mature vestibular hair cells retain capabilities for structural plasticity manifested through modulation of synapse density. Investigations are ongoing that are testing the hypothesis that synapse density increases may result from exposure to centrifugation-induced hypergravity, which would provide the foundation for future research into the molecular mechanisms through which these modifications are induced. This research will provide insight and strategies for inner ear rehabilitation through the induction of synapse density increases in conditions of vestibular paresis.

Maybe zero gravity will play a role in therapies for hearing loss?

Small Molecules-Peptides for Neuroscience Research

Agonists, Antagonists, Inhibitors and Ligands for Studying Neuromodulation

Our friends at R and D Systems/Tocris Bioscience have made available to us select Small Molecules/Peptides. Our focus will be on providing agonists, antagonists, inhibitors and ligands that complement our Neuroscience and Pain Research products and expertise.

2-APB=TRP Channel Modulator

We will be adding about 10 new molecules/peptides per month. Here's a sampling our our most recent additions:

Name	Type	Bioactivity
(±)-trans-ACPD	Agonist	Potent NMDA agonist. Also group II mGluR agonist
(S)-(-)-5-Fluorowillardiine	Agonist	Very potent AMPA agonist
(S)-4-Carboxyphenylglycine	Antagonist	Competitive group I mGluR antagonist/weak group II agonist
2-APB	Modulator	TRP channel modulator. Also IP3 receptor antagonist
2-Methylthioadenosine triphosphate tetrasodium salt	Agonist	P2 purinergic agonist
AM 404	Modulator	Vanilloid receptor agonist. Also anandamide transport inhibitor
BRL 52537 hydrochloride	Ligand	Potent and selective κ opioid receptor agonist
CNQX	Antagonist	Potent AMPA/kainate antagonist
Clocinnamox mesylate	Antagonist	Irreversible μ-opioid receptor antagonist
Endomorphin-1	Agonist	Potent and selective μ opioid receptor agonist
Endomorphin-2	Agonist	Potent and selective μ opioid receptor agonist
FIT	Agonist	Irreversible δ opioid receptor agonist
GBR 13069 dihydrochloride	Agonist	Potent dopamine uptake inhibitor
L-NIO dihydrochloride	Inhibitor	Potent eNOS inhibitor
L-Quisqualic acid	Agonist	Very potent group I mGluR agonist
N-Benzylnaltrindole hydrochloride	Agonist	Opioid receptor selective non-peptide antagonist
Nociceptin	Inhibitor	Endogenous NOP agonist
O-Phospho-L-serine	Antagonist	Group III mGluR agonist; enhances neuronal differentiation
Ro 51	Antagonist	Potent P2X3, P2X2/3 antagonist
cis-ACPD	Agonist	Potent NMDA agonist. Also group II mGluR agonist

We will be posting new additions and related data and publications

mGluR Antibodies in Action

Metabotropic glutamate receptors (mGluRs) are involved in normal brain function and can be perturbed in many neuropathologic conditions. This makes mGluR Markers important tools for Neuroscience Research.

Neuromics has a comphrensive catalog of these markers. They are widely used and frequently reference in pubs-Neuromics' mGluR customer publications. I get excited when a mGluR we recently manufactured is referenced in a publication: Hoon Shim, Chih-Ting Wang, Yen-Lin Chen, Viet Q. Chau, Kevin G. Fu, Jianqi Yang, A. Rory McQuiston, Rory A. Fisher, and Ching-Kang Chen. Defective Retinal Depolarizing Bipolar Cells (DBCs) in Regulators of G-protein Signaling (RGS) 7 and 11 Double Null Mice. JBC Papers in Press. Published on February 27, 2012 as Manuscript M112.345751. The latest version is at http://www.jbc.org/cgi/doi/10.1074/jbc.M112.345751...Animals were sacrificed by CO2 inhalation and the eyeballs were immediately enucleated. After removal of cornea and lens the resulting eyecups were immersionfixed in 4% paraformaldehyde in 1X PBS at room temperature for 15 minutes. This short fixation time ensured good mGluR6 and Gb5 signals at the OPL. After cryoprotection in 30% sucrose in 1X PBS, the eyecups were embedded in TBS (Richard Allan Scientific, Kalamazoo, MI), sectioned at 20μm thickness, and stained...

Images: Absence of Gb5 immunoreactivity in mGluR6-containing puncta in retinas of RGS7 and RGS11 double knockout (711dKO) mice. Retinal sections from wild-type control (WT) and 711dKO (DKO) mice stained for metabotropic glutamate receptor 6 (mGluR6, 1:200) and Gb5 (CT215, 1:250) demonstrates superimposed signals in the WT but absence of Gb5 signal in the DKO. Scale bar equals 10μm.

I will continue to post new developments reagrding this important category of Neurotransmission Research Antibodies.

TrkB and Assembly/Maintenance of GABAergic Neurons

Publications that provide unique insight into neuro-and synptogenesis catch my attention.

This publication focuses on the mechanisms that direct inhibitory circuits. Specifically, the authors study assembly and maintenance of GABAergic inhibitory synapses between Golgi and granule cells in the mouse cerebellar cortex.

Albert I. Chen, Cindy N. Nguyen, David R. Copenhagen, Sylvia Badurek, Liliana Minichiello, Barbara Ranscht, and Louis F. Reichardt. TrkB (Tropomyosin-Related Kinase B) Controls the Assembly and Maintenance of GABAergic Synapses in the Cerebellar Cortex . The Journal of Neuroscience, 23 February 2011, 31(8): 2769-2780; doi: 10.1523/​JNEUROSCI.4991-10.2011.

Our cell adhesion marker-Contactin-1 was referenced: Immunohistochemistry 1:1,000; western blot: 1:1,000

Conclusion Highlights:  Kinase activity of TrkB is required not simply to initiate GABAergic synapse formation, but also to maintain these synapses in adulthood. We also show that the localization of Contactin-1 at the synaptic contacts between Golgi and granule cells requires TrkB suggesting that TrkB promotes synapse formation and maintenance, in part, by controlling the localization of cell adhesion molecules.

Related Reagents:

• Contactin-1, FC Chimera Recombinant Protein
• Contactin-4 Recombinant Protein
• Caspr2 Antibody  
• Axon Growth and Guidance Research
  Antibodies
• Axonal Growth and Guidance Research
  Recombinant Proteins
• Oligodendrocyte or Oligodendroglial Markers
• Primary Neurons and Astrocytes-Primary
  human, rat and mouse neurons and astrocytes 

CAMKIIs and Neurotransmitters.

Here's an update on recent developments. First, we wanted to share a recent publication referencing 2 of our Neurotransmission Research Antibodies:

Haifeng Zhaoa, Qiong Li, Xinrong Pei, Zhaofeng Zhang, Ruiyue Yang, Junbo Wang and Yong Li. Long-term ginsenoside administration prevents memory impairment in aged C57BL/6J mice by up-regulating the synaptic plasticity-related proteins in hippocampus. Behavioural Brain Research Volume 201, Issue 2, 12 August 2009, Pages 311-317. doi:10.1016/j.bbr.2009.03.002. ...anti-phospho-CaMKII (Thr286) and anti- CaMKII (Neuromics, USA)...

Second, we continue to bulk up on reagents for Neurotransmission, Neuromodulation and Synaptic Plasticity Research Reagents. Check out these product categories:

Biogenic Amines
Calcium Signaling
G-Protein Coupled Receptors
Ligand-gated Ion Channels
Transient Receptor Potential Channels
Other Neurotransmitters

Primary Rat, Human and Mouse Neurons and Astrocytes